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Significance We report the identification of anN -ethyl-N -nitrosourea–induced, nonsynonymous mutation in the fumarylacetoacetate hydrolase (Fah ) gene in mice that results in increased plasma tyrosine (chronic tyrosinemia) due to reduced FAH activity in the liver and kidney. Importantly, in contrast to the lethality previously reported with otherFah mutations, our mutant mice survived into adulthood, making them a useful model for examining the long-term behavioral and physiological effects of chronic tyrosinemia.

Tissue-specific FAH deficiency alters sleep–wake patterns and results in chronic tyrosinemia in mice